What are the clinical manifestations of Klinefelter’s syndrome?

  Klinefelter syndrome (47, XXY) is caused by the failure to separate the neutral chromosomes during meiosis (40% occur during spermatogenesis and 60% during oogenesis); chimeric Klinefelter syndrome (46, XY/47, XXY) is caused by the failure to separate the neutral chromosomes during mitosis of the fertilized egg, and chimeric Klinefelter syndrome accounts for about 10% of cases. The incidence of Klinefelter syndrome ranges from 1 in 1000 to 1 in 500. The Klinefelter syndrome phenotype is male and typically presents with small, hard testes (median testicular volume of 4 ml), gynecomastia and high gonadotropins. Some studies suggest that the incidence of breast cancer is more than 50 times higher in patients with Klinefelter syndrome than in normal men. Serum testosterone levels are reduced in 50% to 75% of typical Klinefelter syndrome patients, and serum FSH and 80% of serum LH levels are elevated in 90%. Estradiol is elevated due to aromatization of androstenedione in the surrounding adipose tissue, and the increased estradiol/testosterone ratio causes gynecomastia. Testicular biopsy shows generalized sclerosis of the varicocele with occasional individual varicocele containing supporting cells and spermatozoa.  Low androgen problems: If testosterone is low, it can be supplemented with testosterone’s. The purpose of testosterone supplementation is not to improve fertility, but for one’s own health (sexual life and health problems in other body systems). Under physiological condition, male androgens secrete more in the morning and less in the afternoon, so generally take two capsules in the morning and one in the afternoon; when reviewing, blood should be drawn in the morning; taking it after meals is conducive to the absorption of drugs. However, patients who want to perform microscopic sperm extraction should not take androgen supplementation.